How does the brain fi lter incoming sensory information so that sights and sounds do not become all mixed
together? What happens when the brain loses this fi ltering ability as a result of, say, taking a hallucinogenic drug? What have we learned about depression and anxiety from the drugs that we administer to treat these disorders? The answers to these questions are slowly being revealed as more becomes known about the
actions of serotonin in the brain. Serotonin is a very ancient neurotransmitter and has been found in the venom of amphibians, wasps, and scorpions and within the nematocysts of the sea anemone as well as in the
nervous system of parasitic fl atworms, crickets, and lobsters. Within the human body, 90 %of the total serotonin is contained within the neurons of the gut and is released from the intestines to determine bone growth or shrinkage. Another 8 %of the body’s serotonin is found in the blood and is localized inside
platelets and mast cells; in fact, it was initially discovered in serumand determined to have tonic(or constricting) effects on the vascular system — hence its name. The remaining few percent is found in the brain, in roughly the same location as in every other vertebrate brain, leading scientists to conclude that this neurotransmitter system was present in the primitive nervous system at least one half-billion years ago.
Neurons that produce and release serotonin in the brain are organized into a series of nuclei that lie in a chain along the midline, or seam, of the brainstem; these are called the raphe nuclei (raphe means seam in Latin). These neurons project their axons to every part of the brain, and some of these axons make contact with blood vessels; the neurons also project downward into the spinal cord. If you were able to insert a recording device into the major raphe nuclei and “listen” to the activity of your serotonin neurons, you would discover that they have a regular slow spontaneous level of activity that varies little while you are awake. When you fall asleep, the activity of these neurons slows. When you start to dream — or if, as we’ll see shortly, you ingest a hallucinogen — these neurons cease their activity completely. Despite the relative scarcity of serotonin in your brain, drugs that alter serotonin function can produce profound changes in how you feel and how you experience the world around you. For example, such drugs often stimulate the sympathetic autonomic nervous system and produce increased heart rate, increased respiration, dilated pupils, and other unpleasant side effects. On the other hand, the effects of serotonin upon blood vessel dilation may underlie the ability of an entire class of drugs, known as the tryptans, to attenuate the pain associated with a
migraine headache. Other drugs can also help alleviate symptoms that often accompany migraines and that involve serotonin: depression and sleep problems. The production of serotonin requires the absorption of the
amino acid tryptophan from your food. Transport of this amino acid is influenced by the level of other amino acids in your blood; that level, in turn, is also influenced by what you eat. Within the neurons of your brain, tryptophan is converted to 5-hydroxy-tryptophan by tryptophan hydroxylase, an enzyme that is usually not saturated with substrate. Therefore, if you eat less tryptophan, your brain generally produces less serotonin.
Conversely, providing additional tryptophan in the diet may lead to increased production of serotonin within neurons. It is worth noting, however, that simply producing more of any neurotransmitter does not guarantee that the neuron will actually release it. If too much serotonin is produced, then the excess is
simply discarded. Studies have shown that only extreme depletion or supplementation of this amino acid in the diet can influence serotonin-controlled brain processes such as mood and sleep.
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